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Motion blindness found in some dyslexics

Several years ago, I worked as a clinician at a treatment program for adults with learning disabilities, many of whom were diagnosed with dyslexia; a disorder that negatively impacts a person's ability to read, perceive speech, remember language, and recognize/manipulate language-based sounds. Many of my patients had difficulties advancing in their jobs, struggled to pay the rent or perform daily financial tasks that required reading, and thus relied on others to get by. The countless stories I listened to were heart-breaking, especially when one highly motivated and bright young adult became tearful while relaying to me his strong desire to advance in his career and to make something of himself, but struggled because he couldn't find a way around having to read on the job, no matter what compensatory strategies he used.

Approximately 5 to 17% of the entire population are estimated to have dyslexia. Some famous individuals with dyslexia include Albert Einstein, Whoopi Goldberg, Orlando Bloom, Cher, and Scott F. Fitzgerald. As dyslexia can be inherited, a few of these individuals may have had alterations in a gene known as DCDC2, for which deletion of this gene has been found to be a risk factor for dyslexia. It turns out, they may have also had issues with motion detection.

Cicchini and colleagues (2015), in a recent study published in The Journal of Neuroscience, found that dyslexic individuals who inherited this particular phenotype were found to have impairments for motion processing at high spatial frequencies compared to dyslexics who had the DCD2 gene.

The authors recruited 10 young adult subjects for the experimental group (dyslexics without the DCD2 gene) and 11 for the control group (dyslexics with the DCD2 gene). They then had the subjects fixate on the center of a computer screen while reporting whether they saw patterned black and white lines move from left to right or top to bottom.

Those who lacked the DCD2 gene virtually demonstrated motion blindness. The authors propose that these deficits may be due to anatomical deficits of the lateral geniculate nucleus magnocellular cells (important for vision) as a consequence of DCD2 deletion.

It's a good thing Legolas didn't seem to share the same genetic fate as the experimental group. Otherwise, he'd really be screwed. Legolost? ::rimshot, crickets chirping::